RESUMO
The adverse consequences resulting from diabetes are often presented as severe complications. Diabetic wounds are one of the most commonly occurring complications in diabetes, and the control and treatment of this is costly. Due to a series of pathophysiological mechanisms, diabetic wounds remain in the inflammatory phase for a prolonged period of time, and face difficulty in entering the proliferative phase, thus leading to chronic non-healing wounds. The current consensus on the treatment of diabetic wounds is through multidisciplinary comprehensive management, however, standard wound treatment methods are still limited and therefore, more effective methods are required. In recent years, defensins have been found to play diverse roles in a variety of diseases; however, the molecular mechanisms underlying these activities are still largely unknown. Defensins can be constitutively or inductively produced in the skin, therefore, their local distribution is affected by the microenvironment of these diabetic wounds. Current evidence suggests that defensins are involved in the diabetic wound pathogenesis, and can potentially promote the early completion of each stage, thus making research on defensins a promising area for developing novel treatments for diabetic wounds. In this review, we describe the complex function of human defensins in the development of diabetic wounds, and suggest potential thera-peutic benefits.
RESUMO
OBJECTIVE: To investigate the possible relationship between liver-specific insulin-like growth factor I (IGF-1) and the pathogenesis of breast cancer. METHODS: Fifty non-IGF-1 deficient (LID) mice were randomly divided into 2 equal groups: Group I, fed with dimethyl-benzanthracene (DMBA) for 8 weeks to cause mammary cancer, and Group III, fed with DMBA and ginsenoside Rg for 28 d; and 50 LID mice were randomly divided into 2 equal groups too Group II, fed with DMBA for 8 weeks, and Group IV, fed with DMBA and ginsenoside Rg for 28 d. The mice were killed after the cessation of DMBA use. The serum IGF-1 expression was detected with method Six Gene chips were used to detect the gene expression in the breast cancer tissues. RESULTS: The breast cancer rates were 66.67% in Group I and 33.33% in Group II, 36.00% in Group III, and 12.00% in Group IV. The tumor size was (0.79 +/- 0.20) cm in Group I, (0.37 +/- 0.08) cm in Group III , (0.32 +/- 0.08) cm in Group II, and (0.15 +/- 0.05) cm Group IV. The IGF-1 level of Group II was (41.33 +/- 7.52) ng/ml, 1/4 as high as that of Group I [(166.51 +/- 12.32) ng/ml], and the IGF-1 level of Group IV was (33.48 +/- 6.73) ng/ml, 1/4 as high as that of Group III [(155.84 +/- 11.34) ng/ml]. Compared with those of the control mice, the breast cancers of the LID mice had longer latency, lower incidence, and slower growth rate. The differential gene expression in different serum IGF-1 levels involved binding, metabolism, apoptosis, cell cycle, signal transduction, immune response, transcription regulation and interpretation regulation and so on. Among these genes, Col11, Egln3, Glycam1, Irf6, Lgals7, Perp, Rag1, and Rbm35a genes were closely related to the incidence of breast cancer. CONCLUSION: IGF-1 plays a role as a risk factor in the onset and development of breast cancer by affecting the expression of many differentially expressed genes.
